Axoplasmic transport of proteins labelled by prior incorporation of tritiated amino acids has been examined. We find that: 1. the protein nerve growth factor alters the rate of axoplasmic transport in postganglionic sympathetic fibers of the mouse, and may function as a molecule which controls in vivo transport in these neurons; 2. putrescine, although not itself transported, is effective as an inhibitor of fast axoplasmic transport; 3. over 60 proteins can be defined in the fast transport to the optic relay nuclei, and those transported to the lateral geniculate nucleus cannot be differentiated from those transported to the superior colliculus; 4. a diurnal rhyttm which affects incorporation of amino acids into proteins can alter the amount of tritiated precursor committed to transport; and 5. material carried by rapid axoplasmic transport is associated with lipoprotein aggregates, related to but not identical with the plasma membrane. Antimitotic drugs block transport. Study of podophyllotoxin, picropodophyllin, colchicine, lumicolchicine, and some of the Vinca alkaloids indicates that this inhibition involves an interaction with microtubule protein, or a very similar molecule. Finally, the action of black widow spider venom on the storage and release of acetylcholine has been studied. Three components can be described, of which two appear useful for future study of the process of release.